Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Jun 29;5:635. doi: 10.1038/s42003-022-03578-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 7 — Children born from mothers with GDM experience increased risk of developing T2DM, hypertension, and cardiovascular disease later in life. Key to this enhanced risk is stress-induced dysfunction of vascular progenitor cells, including ECFCs. Cord blood-derived ECFCs isolated from patients with GDM overexpress TAGLN, demonstrate reduced cell migration, and exhibit impaired tube formation compared to normal ECFCs. Cell surface conjugation with bioactive nanoparticles enable pseudo-autocrine stimulation of GDM-ECFCs with SB-431542. Rejuvenation of GDM-ECFCs normalizes TAGLN expression, preserves key progenitor phenotypes, improves cell migration and tube formation in vitro, as well as augments the density and area of chimeric vessels formed in vivo. This cell surface conjugation strategy to rejuvenate GDM-ECFCs and improve their clinical potentials can be used for therapeutic vasculogenesis to address various complications precipitated from GDM.